BCR

Overview

BCR (breakpoint cluster region) encodes a multi-domain signaling protein most notable as the translocation partner of ABL1 in the BCR–ABL1 fusion (Philadelphia chromosome). In AML, BCR–ABL1 is a rare but recurrent RNA-seq-detectable in-frame fusion associated with activated-signaling driver categories.

Alterations observed in the corpus

  • BCR–ABL1 — recurrent in-frame fusion detected by RNA-seq in 200 adult de novo AML cases (TCGA laml_tcga_pub); listed among additional recurrent fusions alongside NUP98–NSD1 and PICALM–MLLT10. PMID:23634996
  • Referenced in HCC targeted therapy resistance analogy context (BCR-ABL/imatinib model informs combination regimen design for HCC) PMID:24735922
  • BCR-ABL1 fusion detected as a BCR-ABL1-like RNA-seq signature in a 9-year-old girl with relapsed/refractory B-cell BLL; addition of dasatinib to third-line induction produced deep remission enabling curative bone-marrow transplant PMID:28007021
  • The BCR–ABL1 fusion is a classic leukemic fusion recovered in LAML ‘fusion-only’ tumors in a pan-cancer RNA-seq fusion analysis across TCGA. PMID:29617662

Cancer types (linked)

  • AML: BCR–ABL1 fusion detected as a recurrent in-frame event in the TCGA AML cohort. PMID:23634996

Co-occurrence and mutual exclusivity

  • BCR–ABL1-fused samples carry fewer cooperating mutations, mirroring the pattern seen in other transcription-factor-fusion AML subgroups. PMID:23634996

Therapeutic relevance

  • The BCR–ABL1 fusion is the canonical target for ABL1 kinase inhibitors (imatinib, dasatinib, nilotinib); clinical utility of TKI therapy in de novo BCR–ABL1+ AML versus blast-crisis CML is not separately addressed in this study. PMID:23634996

Open questions

  • The precise frequency and prognostic significance of BCR–ABL1 within de novo AML (laml_tcga_pub cohort) requires larger-cohort validation. PMID:23634996

Sources

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This page was processed by entity-page-writer on 2026-05-15. - PMID:29617662

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